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Related Concept Videos

Allergic Reactions02:06

Allergic Reactions

Overview
Hypersensitivities01:30

Hypersensitivities

Hypersensitivity, also known as a hypersensitivity reaction or allergic reaction, is a condition where the body's immune system reacts abnormally to a foreign substance. Such substances, that cause hypersensitivity are referred to as an allergen, could be something typically harmless to most people, like pollen or certain foods.
Types of Hypersensitivities
Hypersensitivity reactions are categorized into four types: Type 1, Type 2, Type 3, and Type 4. Each type has a distinct mechanism...
Drug Toxicity: Allergic Reactions01:30

Drug Toxicity: Allergic Reactions

Drug-related allergies are immune-mediated responses triggered by the administration of pharmacological agents. These hypersensitivity reactions are classified based on the immune mechanisms involved. The four primary types—Type I, II, III, and IV—are mediated by different immunological pathways and exhibit distinct clinical manifestations.Type I Hypersensitivity/ IgE-Mediated Reactions: Immunoglobulin E (IgE) immediately mediates Type I hypersensitivity reactions. Upon initial exposure to a...
Allergic Reactions: Anaphylaxis01:30

Allergic Reactions: Anaphylaxis

Anaphylaxis is a severe, life-threatening hypersensitivity reaction mediated by Immunoglobulin E (IgE) antibodies. When IgE binds to allergens, it triggers the release of mediators– histamine, leukotrienes, and prostaglandins from mast cells and basophils. These mediators cause vasodilation, edema, and inflammation, leading to various symptoms.The primary allergens causing anaphylaxis include food items (e.g., peanuts, shellfish), drugs (e.g., penicillin, asparaginase, corticotropin, heparin),...
Hypersensitivity Reactions: Cytolytic Reactions01:01

Hypersensitivity Reactions: Cytolytic Reactions

Type II hypersensitivity involves IgG and IgM antibodies targeting cell surface antigens, leading to cell destruction. This can occur through complement activation, antibody-dependent cell-mediated cytotoxicity (ADCC), or acting as opsonins for phagocytosis. When excessive, these reactions cause significant tissue damage.Drug-induced hemolytic anemia is a common example, where drugs like penicillin or cephalosporins bind to red blood cells, forming drug-protein complexes. These complexes...
Hypersensitivity Reactions: Immune-Complex Reactions01:19

Hypersensitivity Reactions: Immune-Complex Reactions

Type III hypersensitivity reactions occur when antigen–antibody complexes form and activate the complement system. Normally, these complexes help the clearance of antigens by phagocytes and red blood cells. However, when large numbers of immune complexes are present, they can deposit in tissues—particularly in the walls of blood vessels—leading to inflammation and tissue injury. These deposits trigger complement activation and neutrophil recruitment, resulting in serum sickness, a systemic...

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Related Experiment Video

Updated: Jun 25, 2026

Depletion of Specific Cell Populations by Complement Depletion
06:17

Depletion of Specific Cell Populations by Complement Depletion

Published on: February 5, 2010

Acute anaphylaxis associated with serum complement depletion.

H Tannenbaum, S Ruddy, P H Schur

    The Journal of Allergy and Clinical Immunology
    |September 1, 1975
    PubMed
    Summary
    This summary is machine-generated.

    Anaphylaxis after lidocaine injection in a rheumatoid arthritis patient was linked to a complement system abnormality. This endogenous complement defect may have predisposed the patient to the severe allergic reaction.

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    Area of Science:

    • Immunology
    • Rheumatology
    • Pharmacology

    Background:

    • Rheumatoid arthritis (RA) patients may experience adverse drug reactions.
    • Anaphylaxis is a severe, potentially life-threatening allergic reaction.
    • Complement system activation plays a role in inflammatory and allergic responses.

    Purpose of the Study:

    • To investigate the immunological mechanisms underlying anaphylaxis in a patient with rheumatoid arthritis following lidocaine administration.
    • To explore the potential role of complement system abnormalities in the anaphylactic reaction.

    Main Methods:

    • Case report of a 45-year-old woman with RA experiencing anaphylaxis post-lidocaine injection.
    • Analysis of serum complement component levels (CH50, C1q, C1s, C4, C2, C3, C5, C6, C9, Factor B) and C1 inhibitor concentrations.
    • In vitro testing of lidocaine and methylprednisolone acetate for complement activation.
    • Absence of detectable circulating immune complexes and antibodies to lidocaine.

    Main Results:

    • Marked depression of serum complement component levels for 18 hours post-anaphylaxis.
    • Diminished hemolytic activity of complement components C4 and C2, despite normal protein concentrations.
    • Normal or slightly depressed serum C1 inhibitor concentrations.
    • No complement activation observed in vitro with lidocaine or methylprednisolone acetate.

    Conclusions:

    • The patient's anaphylactic reaction to lidocaine may have been influenced by an underlying endogenous complement abnormality.
    • Specific deficiencies in complement component function (C4, C2) might predispose individuals to severe reactions.
    • Further research is needed to elucidate the link between complement system defects and drug-induced anaphylaxis in RA patients.